Endothelial dysfunction and inflammation in different stages of essential hypertension

Abstract

The objective of this study was to assess the various factors affecting endothelial function in essential hypertensives and to establish a relation between them in a regression model. Also, the micro-inflammatory state that is known to exist in essential hypertension was evaluated. Sixty newly detected patients of essential hypertension not on any prior treatment and classified into Stage-1 or Stage-2 hypertension according to the JNC-VII criteria were recruited in the study. After a detailed history and physical examination, investigations including blood urea, serum creatinine, blood sugar (F), S. lipid profile (F), urine for albumin, sugar and sediments, X-ray of the chest, ECG and fundus examination were carried out. Urine for microalbuminuria, Hs-CRP and brachial artery reactivity were tested as markers of endothelial dysfunction and inflammation. The CRP levels, taken as a marker of inflammation in hypertension, were significantly elevated in a majority of the study subjects. Endothelial dysfunction was significantly more quantified in Stage-2 hypertension as compared with Stage-1 hypertension (P < 0.01). The Hs-CRP levels were consistently found to be elevated in both the stages of hypertension in our study, with an insignificant difference between the two groups. A significant association was noted with the stage of hypertension, triglycerides, microalbuminuria, CRP, LDL cholesterol and age, with the stage of hypertension emerging as the most powerful predictor variable (P < 0.0001) followed closely by microalbuminuria (P < 0.0001) in a multiple regression analysis model. The present study reinforces the view that hypertension is in part an inflammatory disorder. Endothelial dysfunction is an important component of essential hypertension, the severity being determined by the stage of hypertension, microalbuminuria, LDL-cholesterol, triglycerides, age and Hs-CRP levels independently. The undesirable inflammatory response can be cost-effectively prevented at various levels by targeting the potentially modifiable risk factors elucidated in the study.